Objective To explore the protective effect of atorvastatin on irradiated endothelium and the thrombomodulin(TM)expression.Methods Cultured human coronary artery endothelial cells(HCAEC)and human umbilical vein endothelial cells(HUVEC)were treated by atorvastatin at the final concentration of 10 μmol/ml for 10 min,and then irradiated with 2 and 25 Gy.Cell cycles status and TM expression were quantitatively measured by flow cytometry 24 hours after irradiation.Protein C activation in endothelial cells was also assessod.Results After administration with atorvastatin for 24 h,the TM expression increased by 77%,59% and 61% in normal control group,2 Gy group and 25 Gy group,respectively(t=27.395,26.420,58.065;P=0.000).The protein C levels decreased by 23% and 34% compared with the normal group post-irradiation to 2 and 25 Gy,but increased by 79% and 76% compared with the irradiated control group after administration with atorvastatin.The rates of cell apoptosis decreased by 6% and 16% in 2 Gy and 25 Gy groups,respectively after administration with atorvastatin for 24 h(t=4.178,17.863;P=0.000).Conclusions Atorva statin can protect endothelia cell from irradiation-induced apeptosis by increasing TM expression and protein C activation.

Objective: To discuss the significance of neoadjuvant chemotherapy followed by surgery in the treatment of local advanced esophageal cancer. Methods:A total of 272 cases of local advanced esophageal cancer were studied in retrospect. Out of the 272 cases, 112 were treated with neoadjuvant chemotherapy followed by surgery (CT-S), whereas the remaining 160 cases underwent surgical treatment (S) only. Complications and survival state after surgery were compared. Results: The rate of complications after surgery was as follows: CT-S: 34.8% (39/112); S: 29.4% (47/160), P=0.50. The five-year survival rate was 35.7% and 29.4%, respectively, P<0.05. The CT-S patients were divided into partial remission (PR) and stable disease (SD)/progressive disease (PD) groups according to the effect of the chemotherapy. The five-year survival rate was 38.5% and 30.1%, respectively, P<0.01. Conclusion: Neoadjuvant chemotherapy is available for local advanced esophageal cancer. Postoperative complications are not increased by chemotherapy, and the survival rate for local advanced esophageal cancer is improved by neoadjuvant chemotherapy. PR has better prognosis compared with SD/PD.

AIM:To investigate the effects of down-regulated miR-9 expression on the proliferation , invasion and migration of nasopharyngeal carcinoma (NPC) cells.METHODS:Human NPC CNE1 and CNE2 cells were transfect-ed with the inhibitor of miR-9 by Lipofectamine to down-regulate the expression of miR-9, and the cells transfected with an inhibitor control were also set up .The cell proliferation and cell cycle were evaluated by CCK-8 assay and flow cytometry . The cell invasion and migration abilities were detected by Transwell invasion and wound -healing assays .Immunoblotting was applied to analyze the levels of the proteins .RESULTS:Compared with control group , inhibition of miR-9 expression in the NPC cells by transfection of the miR-9 inhibitor significantly decreased the proliferation ability (P<0.05).The per-centages of the cells in G 0/G1 phase [ CNE2: ( 57.96 ±1.39 )% vs ( 47.93 ±1.76 )%, P<0.05; CNE1: ( 51.24 ± 0.88)%vs (48.29 ±0.39)%, P<0.05] were significantly increased.The migration distances [CNE2: (186.50 ± 7.94)μm vs (247.56 ±15.56)μm, P<0.05;CNE1:(139.06 ±16.73)μm vs (230.66 ±14.27)μm, P<0.01] and the invasion ability of the CNE2 cells (43.00 ±3.17 vs 65.80 ±5.20, P<0.01) were also significantly inhibited .Moreo-ver, the tumor cells transfected with the inhibitors produced lower β-catenin.CONCLUSION:Inhibition of miR-9 expres-sion suppresses the proliferation , invasion and migration of nasopharyngeal carcinoma cells .

OBJECTIVETo investigate the effects of down-regulated miR-9 expression on ultraviolet rays (UV)-induced reactive oxygen species (ROS) damage in nasopharyngeal carcinoma (NPC) cells.

METHODSThe NPC cells were transfected with inhibitors of miR-9 by lipofectamine to decrease the expression of miR-9, and the cells transfected with inhibitor control as the control. ROS levels following UV exposure were examined with DCF-DA method and the concentration of glutathione was analyzed via the benzoic acid method; DNA damage and apoptosis also were evaluated.

RESULTSThere was significant difference in ROS levels between miR-9 expression-inhibited cells and control cells (26 895 ± 218 vs 15 765 ± 927, t = 39.754, P < 0.001), and also there were significant differences in DNA damage rates (28.0% ± 10.0% vs 23.6% ± 9.2%) and in apoptosis rates (8.0% ± 0.9% vs 4.5% ± 0.8%) following UV exposure between two groups of cells. The miR-9 expression-inhibited cells showed lower level (1.87 ± 0.15) µmol/L of glutathione compared with the control cells (9.85 ± 0.15) µmol/L (t = -48.832, P < 0.001).

CONCLUSIONInhibition of miR-9 expression promoted UV-induced ROS damage in nasopharyngeal carcinoma cells.

Apoptosis ; Carcinoma ; Cell Line, Tumor ; DNA Damage ; Humans ; MicroRNAs ; metabolism ; Nasopharyngeal Neoplasms ; metabolism ; Reactive Oxygen Species ; metabolism ; Transfection

With the increasing aging population, the incidence of wet age-related macular degeneration(wARMD)is gradually rising. The formation of neovascularization leads to recurrent hemorrhage in the macular region, which is one of the main causes of blindness in the elderly. Currently, the primary clinical treatment for wARMD is intravitreal injection of anti-vascular endothelial growth factor(VEGF)drugs. However, there are still some patients who have poor or no response to anti-VEGF drugs, resulting in suboptimal or ineffective clinical outcomes. Analyzing the specific influencing factors will be beneficial in guiding clinical decision-making. This article reviews the impact of factors such as advanced age, treatment duration, number of injections, characteristics of neovascular lesions, macular structure, intraocular cytokine levels, and genetics on the response to anti-VEGF therapy. In addition, recent studies have found that pericytes, as cellular components of microvascular walls, can influence the sensitivity to anti-VEGF therapy. This review summarizes the current research on the mechanisms of pericytes in poor or non-response to anti-VEGF therapy and discusses targeted strategies focusing on pericytes.

OBJECTIVETo observe the clinical therapeutic effects of sternoclavicular hook plate for the treatment of sternoclavicular joint dislocation.

METHODSFrom June 2010 to June 2012, 7 patients with sternoclavicular joint dislocation were treated with sternoclavicular hook plate fixation. Among the 7 patients, 5 patients were male and 2 patients were female, and the average age was 42.3 years, ranging from 38 to 54 years. The course of the disease ranged from 1 to 4 weeks. All the patients had trauma history. The clinical manifestations included: obvious swelling and pain of sternoclavicular joint, restricted shoulder joint activity. The sternoclavicular joint dislocation was proved by preoperative X-ray and CT. The postoperative curative effect was evaluated according to Rockwood scoring method.

RESULTSAccording to Rockwood scoring method, the excellent results obtained in 6 cases, good in 1. There were no complications such as internal fixation loosening or broken, second dislocation, pain in the sternoclavicular joint, and deformity. The function of shoulder joint was good, and the limb activity was free and no pain appeared.

CONCLUSIONThe sternoclavicular hook plate for the treatment of sternoclavicular joint dislocation has follow advantages: simple procedure, stable fixation, definite therapeutic effects.

Adult ; Female ; Fracture Fixation, Internal ; methods ; Humans ; Joint Dislocations ; diagnostic imaging ; surgery ; Male ; Middle Aged ; Radiography ; Sternoclavicular Joint ; injuries ; surgery

OBJECTIVETo explore the role of sonic hedgehog (Shh) pathway in regulating the proliferation, migration and differentiation of hemangioblasts derived from aorta-gonad-mesonephros (AGM).

METHODSThe hemangioblasts were isolated from AGM region of 11-day postcoitum (dpc) murine embryos by using the immuno-magnetic with CD34 and Flk1 monoclonal antibodies. The phenotypic analysis of hemangioblasts and AGM-derived stromal cells were detected by flow cytometry. The secretion of Shh was examined by immunohistochemical staining. The roles of Shh in regulating the proliferation, migration and differentiation of hemangioblasts in the transwell non-contact coculture system with AGM-derived stromal cells were observed by adding exogenous Shh N-Terminus and its antibody.

RESULTSThe protein of Shh was highly expressed on AGM-derived stromal cells. The proliferation of hemangioblasts was promoted when co-cultured with AGM-derived stromal cells, and the effects of the latter could be blocked by antibody of Shh. The proliferation of hemangioblasts was strengthened further and kept for a long time without differentiation and apoptosis when exogenous Shh N-Terminus was added into the transwell non-contact co-culture system with AGM-derived stromal cells. When exogenous Shh N-Terminus was added into the cultural supernatant of hemangioblasts without AGM-derived stromal cells, the hemangioblasts were observed to be induced to apoptosis or differentiation after a short time of proliferation. Furthermore, the ability of migration could be promoted in the co-cultured hemangioblasts by adding exogenous Shh N-Terminus.

CONCLUSIONShh pathway probably involves in the regulation of the proliferation, differentiation, apoptosis and migration of hemangioblasts, and is regulated by the AGM microenvironment.

Adrenal Glands ; cytology ; Animals ; Aorta ; cytology ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Embryo, Mammalian ; cytology ; Hedgehog Proteins ; metabolism ; Hemangioblasts ; metabolism ; physiology ; Mesonephros ; cytology ; Mice ; Mice, Inbred BALB C ; Signal Transduction

OBJECTIVETo investigate the role of Mcl-1 gene in resistance of all-trans retinoic acid (ATRA) of leukemia cells.

METHODSLong-term, intermittent and repetitive exposure of HL-60 cells to ATRA was used to establish a multidrug-resistance cell line (HL-60/ATRA). HL-60/ATRA cells were transfected with Mcl-1 small interference RNA (siRNA) by Lipofectamine 2000. Western blot was used to detect the expression of Mcl-1. The proliferation, apoptosis and differentiation were evaluated by MTT assay, in situ nick end-labeling (TUNEL) and NBT assay, respectively.

RESULTSThe HL-60/ATRA could keep its undifferentiated and proliferative status to a high concentration of ATRA (100 nmol/L) with highly expressed Mcl-1 protein (relative grey scale 0.624 +/- 0.127). Mcl-1 gene knockdown by siRNA (relative grey scale 0.267 +/- 0.086) could reverse the resistance of ATRA of HL-60/ATRA by inhibiting proliferation, and inducing differentiation and apoptosis [apoptosis rate (18.5 +/- 4.5)%].

CONCLUSIONMcl-1 gene might be involved in ATRA resistance in HL-60 cells and inhibiting its expression could be a new approach to ATRA resistance reversion.

Apoptosis ; drug effects ; genetics ; Cell Differentiation ; drug effects ; genetics ; Cell Proliferation ; drug effects ; Drug Resistance, Neoplasm ; genetics ; HL-60 Cells ; drug effects ; metabolism ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; RNA, Small Interfering ; Tretinoin ; pharmacology

Hemorrhagic shock (HS) is one of the leading causes of death among young adults worldwide. Multiple organ dysfunction in HS is caused by an imbalance between tissue oxygen supply and demand, which is closely related to the poor prognosis of patient. Mitochondrial dysfunction is one of the key mechanisms contributing to multiple organ dysfunction in HS, while mitochondrial quality control regulates mitochondrial function through a series of processes, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mitochondrial-derived vesicles, and mitochondrial protein homeostasis. Modulating mitochondrial quality control can improve organ dysfunction. This review aims to summarize the effects of mitochondrial dysfunction on organ function in HS and discuss the potential mechanisms of mitochondrial quality control, providing insights into the injury mechanisms underlying HS and guiding clinical management.

BACKGROUNDAmerican College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines gave fondaparinux a class I recommendation for use in patients with non-ST elevation acute coronary syndromes (NSTE-ACS) undergoing invasive or conservative strategy. Nadroparin is one of the common anticoagulants used in NSTE-ACS in China. Accordingly, this study compared the safety and efficacy between fondaparinux and nadroparin in patients with NSTE-ACS.

METHODSIn this prospective, randomized, open-label, and single center study, a total of 300 patients with NSTE-ACS were randomized to receive either fondaparinux (group F, n = 150, 2.5 mg/d) or nadroparin (group N, n = 150, 0.1 ml/10 kg q12 h) for a mean of 4 days. The primary safety endpoint was the incidence of major or minor bleeding at 9 days that was not related to coronary artery bypass grafting (CABG). The primary efficacy endpoints included death, myocardial infarction, or recurrent ischemia at 9 days. All patients underwent a 180-day follow-up.

RESULTSBaseline characteristics were well matched between the two groups. There was a non-significant 28% relative risk reduction in the primary safety endpoint in group F compared with group N (4.7% vs. 6.7%, HR 0.72, 95%CI 0.42-1.65, P = 0.38). The primary efficacy endpoint was 8.0% in group F and 10.0% in group N (HR, 0.82, 95%CI 0.54-1.71, P = 0.49). The composite of the safety and efficacy endpoints at 9 days (10.0% vs. 16.0%, HR 0.61, 95%CI 0.31-1.10, P = 0.10), 30 days (14.0% vs. 17.9%, HR 0.72, 95%CI 0.47-1.16, P = 0.21), or 180 days (18.7% vs. 27.3%, HR 0.65, 95%CI 0.38-1.11, P = 0.11) showed a non-significant trend toward a lower value in group F.

CONCLUSIONFondaparinux resulted in a nonsignificant risk reduction in patients with NSTE-ACS in both bleeding and ischaemic events during short- and long-term follow-up compared with nadroparin.

Acute Coronary Syndrome ; drug therapy ; Aged ; Anticoagulants ; adverse effects ; therapeutic use ; Female ; Fibrinolytic Agents ; adverse effects ; therapeutic use ; Humans ; Male ; Middle Aged ; Nadroparin ; adverse effects ; therapeutic use ; Polysaccharides ; adverse effects ; therapeutic use ; Treatment Outcome